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Amphiregulin Induces iNOS and COX-2 Expression through NF-B and MAPK Signaling in Hepatic Inflammation.
Mediators Inflamm
November 2023
Department of Endocrinology and Metabolism, Ajou University School of Medicine, 206, World cup-ro, Yeongtong-gu, Suwon 16499, Republic of Korea.
Background: Inflammation is a major cause of hepatic tissue damage and accelerates the progression of nonalcoholic fatty liver disease (NAFLD). Amphiregulin (AREG), an epidermal growth factor receptor ligand, is associated with human liver cirrhosis and hepatocellular carcinoma. We aimed to investigate the effects of AREG on hepatic inflammation during NAFLD progression, and .
View Article and Find Full Text PDFT cell depletion by cytotoxic elimination.
Curr Protoc Immunol
May 2001
National Cancer Institute, Bethesda, Maryland, USA.
This unit describes the complete removal of T cells from lymphocyte preparations based on the presence of the glycoprotein Thy-1 on the cell surface of T lymphocytes. As in UNIT 3.3, cytotoxic elimination is employed; however, Thy-1-specific antibodies are used rather than MHC class II-specific antibodies so that T cells are eliminated rather than B cells and accessory cells.
View Article and Find Full Text PDFA therapeutic anti-CD4 monoclonal antibody inhibits T cell receptor signal transduction in mouse autoimmune cardiomyopathy.
Chin Med J (Engl)
August 2007
Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Background: T cell immune abnormalities in patients with dilated cardiomyopathy (DCM) has been intensively studied over the past 10 years. Our previous study has suggested that immunization of mice with the peptides derived from human adenine nucleotide translocator (ANT) result in the production of autoantibodies against the ANT and histopathological changes similar to those in human DCM. The ANT peptides can induce autoimmune cardiomyopathy like DCM in Balb/c mice.
View Article and Find Full Text PDFAnalysis of IgG subclass antibodies and expression of T-Cell receptor signaling molecules in anti-CD4 monoclonal antibody treated mice with autoimmune cardiomyopathy.
Autoimmunity
September 2006
Laboratory of Cardiovascular immunology, Tongji Medical College, Institute of Cardiology, Union Hospital, Huazhong Technology and Science University, 1277 Jie-Fang Avenue, Wuhan, 430022, People's Republic of China.
T-cell immune abnormality in patients of dilated cardiomyopathy has been intensively studied over the past 10 years. In this study, we aim to focus on the molecular mechanism of T-cells in autoimmune cardiomyopathy mouse model by detecting the expression of three T-cell signaling molecules. Balb/C mice (n = 12) were immunized with the peptides derived from human ADP/ATP carrier on the 1st, 14th, 28th, 49th and 79th days, and half of them were also injected with anti-L3T4 McAb on the - 1st, 0 and 1st days.
View Article and Find Full Text PDF[Effects of immunotherapy with anti-L3T4 monoclonal antibody on autoimmune cardiomyopathy: experiment with mice].
Zhonghua Yi Xue Za Zhi
December 2005
Institute of Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Objective: To evaluate the effects of immunotherapy with anti-L3T4 monoclonal antibody (McAb) on autoimmune cardiomyopathy.
Methods: 24 male Balb/c mice were immunized with mitochondria ADP/ATP carrier peptides so as to establish a model of autoimmune cardiomyopathy, and then randomly divided into 4 equal groups: cardiomyopathy control group, early-treated group injected with anti-L3T4 McAb on the day before immunization, the very day of immunization, and 1 day after the immunization, mid-term-treated group, administrated with anti-L3T4 McAb on the 89th, 90th and 91st days after immunization, and sham-immunization control group, injected with solution without anti-L3T4 McAb. Six months after blood samples were collected.
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